Log In Sign up
The largest database of trusted experimental protocols

B6 cb17 prkdcscid szj scid mice

Manufactured by Jackson ImmunoResearch
Visit Supplier
Sourced in United States

B6.CB17-Prkdcscid/SzJ Scid mice are a genetically modified mouse strain. The mice have a mutation in the Prkdc gene, which results in a deficiency in DNA-dependent protein kinase activity. This leads to impaired V(D)J recombination and a lack of functional T and B cells, resulting in a severe combined immunodeficiency (SCID) phenotype.

Automatically generated - may contain errors

Lab products found in correlation

Metformin, by Fujifilm (1 mentions) D12331, by Research Diets (1 mentions) C57bl 6jjcl mice, by CLEA Japan (1 mentions)

Spelling variants of this product

SCID mice (40 citations) B6.CB17-Prkdcscid/SzJ (12 citations) CB17 SCID mice (7 citations) B6 scid mice (2 citations)

4 protocols using b6 cb17 prkdcscid szj scid mice

1

Murine Multiple Myeloma Xenograft Model

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
Immune-deficient mice with global deletion of Sost
(Sost−/−/Scid) were generated by crossing
Sost−/− mice (22 (link)) with B6.CB17-Prkdcscid/SzJ Scid mice (Jackson laboratories, Bar
Harbor, Maine, USA). Six-wk-old Sost−/−/Scid and
control littermate mice (wt/Scid) were injected intratibially with
105 human JJN3 myeloma cells or saline and sacrificed 4wks later
(6 (link)). Six to 10 female and male mice
per group were used for these experiments. Six-wk-old immune-competent
C57BLKaLwRij (23 (link), 24 (link)) mice were injected intratibially with
105 murine 5TGM1 myeloma cells or saline. After four weeks, tumor
engraftment was confirmed, mice were stratified by IgG2b levels, and then
control mice and mice bearing MM were treated with either Scl-Ab (15mg/kg/wk) or
control antibody (IgG) for four additional weeks, when the mice were sacrificed.
Seven to 10 female and male mice per group were used for these experiments.
Sample size for these studies was calculated based on previous studies (6 (link), 25 (link)). Mice were fed with a regular diet (Harlan, Indianapolis, IN),
received water ad libitum, and were maintained on a 12-hour light/dark cycle.
Studies were approved by the Institutional Animal Care and Use Committee of the
Indiana University School of Medicine.
Delgado-Calle J., Anderson J., Cregor M.D., Condon K.W., Kuhstoss S.A., Plotkin L.I., Bellido T, & Roodman G.D. (2017). Genetic Deletion of Sost or Pharmacological Inhibition of Sclerostin Prevent Multiple Myeloma-induced Bone Disease without Affecting Tumor Growth. Leukemia, 31(12), 2686-2694.
+ Open protocol
+ Expand
2

Lineage Tracing of Tie2+ Cells in Bone Tumors

Check if the same lab product or an alternative is used in the 5 most similar protocols
TEK-Cre (B6.Cg-Tg12Flv #004128, Jackson laboratory) mice were bred with B6.Cg-Gt(ROSA)26Sor (Rosa-tdTomato) mice (#007914 Jackson Laboratory) to create the Tie2-Cre/Rosa-tdTomato mouse. Male mice were used for in vivo lineage tracing study. Tumor cells were injected into right femur of the mouse. After five weeks, mice were subjected to radiograph. Femurs were fixed in PFA, decalcified in EDTA, and embedded in OCT for cryosections. Mice with the conditional osx allele osxf/f were generated previously (Zhou et al., 2010 (link)). To generate Tie2cre/Osxf/f/SCID mice, we crossed osxf/f mice with B6.CB17-Prkdcscid/SzJ SCID mice (#001913, Jackson Laboratory) and TEK-Cre mice. Genotyping for Tie2-cre and SCID allele was done by PCRs, following the protocols from the Jackson laboratory. Genotyping for conditional osx alleles was performed using the forward primer 5’-CTT GGG AAC ACT GAA GCT GT-3’ and the reverse primer 5’-CTG TCT TCA CCT CAA TTC TAT T-3’ in a PCR reaction of 3 minutes at 95°C, 35 cycles of 30 seconds at 94°C, 30 seconds at 58°C, 1 minute at 72°C, and completed with final extension 5 minutes at 72°C. Both male and female mice were used in xenograft studies.
Lin S.C., Lee Y.C., Yu G., Cheng C.J., Zhou X., Chu K., Murshed M., Le N.T., Baseler L., Abe J.I., Fujiwara K., deCrombrugghe B., Logothetis C.J., Gallick G.E., Yu-Lee L.Y., Maity S.N, & Lin S.H. (2017). Endothelial-to-osteoblast conversion generates osteoblastic metastasis of prostate cancer. Developmental cell, 41(5), 467-480.e3.
+ Open protocol
+ Expand
3

Murine Multiple Myeloma Xenograft Model

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
Immune-deficient mice with global deletion of Sost
(Sost−/−/Scid) were generated by crossing
Sost−/− mice (22 (link)) with B6.CB17-Prkdcscid/SzJ Scid mice (Jackson laboratories, Bar
Harbor, Maine, USA). Six-wk-old Sost−/−/Scid and
control littermate mice (wt/Scid) were injected intratibially with
105 human JJN3 myeloma cells or saline and sacrificed 4wks later
(6 (link)). Six to 10 female and male mice
per group were used for these experiments. Six-wk-old immune-competent
C57BLKaLwRij (23 (link), 24 (link)) mice were injected intratibially with
105 murine 5TGM1 myeloma cells or saline. After four weeks, tumor
engraftment was confirmed, mice were stratified by IgG2b levels, and then
control mice and mice bearing MM were treated with either Scl-Ab (15mg/kg/wk) or
control antibody (IgG) for four additional weeks, when the mice were sacrificed.
Seven to 10 female and male mice per group were used for these experiments.
Sample size for these studies was calculated based on previous studies (6 (link), 25 (link)). Mice were fed with a regular diet (Harlan, Indianapolis, IN),
received water ad libitum, and were maintained on a 12-hour light/dark cycle.
Studies were approved by the Institutional Animal Care and Use Committee of the
Indiana University School of Medicine.
Delgado-Calle J., Anderson J., Cregor M.D., Condon K.W., Kuhstoss S.A., Plotkin L.I., Bellido T, & Roodman G.D. (2017). Genetic Deletion of Sost or Pharmacological Inhibition of Sclerostin Prevent Multiple Myeloma-induced Bone Disease without Affecting Tumor Growth. Leukemia, 31(12), 2686-2694.
+ Open protocol
+ Expand
4

High-fat Diet, Metformin, and Tumor Growth

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
C57BL/6JJcl mice (CLEA Japan, Tokyo, Japan) and B6.CB17-Prkdcscid/SzJ (SCID) mice (The Jackson Laboratory, Bar Harbor, ME) were maintained with free access to chow and water. The mice were fed standard chow diet (STD) (MF, Oriental Yeast, Japan) or high fat-high sucrose diet (HFS: Protein: 16.4% kcal, Fat: 58% kcal, Carbohydrate: 25.5% kcal, Energy Density: 5.56 kcal/g) (D12331, Research Diets, New Brunswick, NJ).
For tumor growth assay, 4-week-old C57BL/6JJcl and B6.CB17-Prkdcscid/SzJ male mice were fed with STD or HFS for 6 weeks and injected with 4 × 105 B6 OVA-gene introduced B16 melanoma MO5 cells. Seven days after injection of MO5 cells, they were divided into 4 groups fed with (1) STD with water (STD), (2) STD with 5 mg/dl metformin (WAKO, Tokyo, Japan) water (STD + Met), (3) HFS with water (HFS), and (4) HFS with 5 mg/dl metformin water (HFS + Met) for 4 weeks. Mice that received metformin at 5 mg/ml achieved 1.70 μg/mL, which was consistent with plasma concentrations in patients (0.5–2 μg/mL)39 (link). Tumor infiltrating lymphocytes (TILs) were isolated at 48 h after the administration of metformin and subjected to cytokine assay.
4-week-old C57BL/6JJcl mice were fed with STD and HFS for 12 weeks and they were divided into STD, STD + Met, HFS, and HFS + Met for 2 weeks. Then, splenocytes were isolated and subjected to cytokine assay and Extracellular Flux Analyzer.
Nojima I., Eikawa S., Tomonobu N., Hada Y., Kajitani N., Teshigawara S., Miyamoto S., Tone A., Uchida H.A., Nakatsuka A., Eguchi J., Shikata K., Udono H, & Wada J. (2020). Dysfunction of CD8 + PD-1 + T cells in type 2 diabetes caused by the impairment of metabolism-immune axis. Scientific Reports, 10, 14928.
+ Open protocol
+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Sign up for free.
Registration takes 20 seconds.
Available from any computer
No download required

Sign up now

Revolutionizing how scientists
search and build protocols!